Assessment and mgmt of pt with liver disorders Flashcards
Liver A+P
- Largest gland in the body
- RUQ (If there is pain in this quadrant it’s probably liver or gallbladder related)
- Very vascular
- Receives blood from nutrient rich blood from GI tract via the portal vein
- Oxygen rich blood from the hepatic artery
- Mix of oxy and deoxy blood with the hepatocytes
Biliary system
- Liver produces bile
- Bile moves into the bile ducts
- Bile moves into the gallbladder for storage or is immediately used
- Bile is them moved to the sphincter of oddi
- Bile is then excreted into the intestine for fat digestion
Obstruction can lead to N+V and overall sickness
Functions of the liver: Glucose
Metabolism and regulation of glucose serum concentration
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Functions of the liver: Ammonia
Converts it into urea
-In liver disease, it prevents the conversion, increasing ammonia levels. Which can be detrimental
Functions of the liver: Protein metabolism
- Formation of albumin, globulins, clotting factors, lipoproteins
What is required for the synthesis of prothrombin and other clotting factors
Vitamin K
Functions of the liver: Vitamin and iron storage
ABD
A/D are Fat soluble vitamins
Functions of the liver: Bile formation
- Water,
- Electrolytes
- bicarb
- lecithin
- fatty acids
- cholesterol
- bilirubin
- bile salts
*
Functions of the liver: Bilirubin excretion
To the gallbladder and intestine
Functions of the liver: Drug metabolism
Metabolizes drugs
First pass effect
First pass effect
Liver almost completely metabolizes a drug the first time it sees it and requires a higher dose for its therapeutic level
Important labs related to the liver
Aminotransferases
* AST
* ALT
* GGT
* LDH
Protein and albumin
Bilirubin
Clotting factors
* PT/INR
* Plt
Ammonia
Lipids
AST> ALT
Myocardial necrosis
ALT> AST
Liver issues
Normal AST
8-48 U/L
Normal ALT
7-55 U/L
Normal ALP
45-115 U/L
Normal bilirubin
0.1-1.2 mg/L
Normal Total protein
6.3-7.9 mg/L
Normal albumin
3.5-5 ml/L
Transaminases
ALT, AST and GTT
Indicators of injury to liver cells, useful in detecting hepatitis
Alanine aminotransferase (ALT)
Increased primarily in liver disorders used to monitor the course of hepatitis, cirrosis and the effectiveness of treatments that may be toxic to the liver
Main one
Transaminase
Aspartate aminotransferase (AST)
Not specific to liver diseases may be increased in cirrhosis, hepatitis, and liver cancer
Will be elevated but not to the degree of ALT
Gamma-glutamyl transferase (GTT)
Associated with cholestasis (Blocked bile), alcoholic liver disease
Diagnostics for liver dysfunction
- Ultrasound
- CT scan
- MRI
- ERCP (Endoscopic retrograde cholangiopancreatography)
- Transient liver elastography (Stiffness of the liver)
- Liver biopsy (Invasive)
Health history liver dysfunction
- Exposure to hepatotoxic substances (Environmental exposures)
- Infections (Hepatitis)
- Travel, substance use disorder
- Lifestyle (High risk behaviors)
- Meds, OTC supplements (Patient won’t tell you all the supplements that they take)
- Familial liver disorders
Physical assessment with liver dysfunction: Skin
- May be pale from anemia
- Jaundice
- Jaundice can lead to pruritus and excoriations
- Peticuli
- Spider angiomas
Physical assessment with liver dysfunction
- Skin
- Cognitive status
- Motor function
- Abdomen: Palpation and percussion
Manifestations of liver disease
- Cognitive changes
- Altered sleep wake
- Gastroesophageal bleeding- hematemesis, melena
- Splenomegaly
- Ascites
- Jaundice
- Petechiae, ecchymosis, nosebleeds
- Palmar erythema
- Spider angiomas
- Dependent peripheral edema of extremities and sacrum
- Asterixis
- Fetor hepaticus
- Gyneo, testicular shrinkage
Asterixis
Coarse tremor that causes a flapping motion of the wrist to occur
Fetor hepaticus
Breath smells fruity, or stool
Why does gyno and testicular shrinkage occur in liver disease
Liver cant break down estrogen leading to increased levels
RUQ pain
Inflammation of the liver, when liver disease progresses and cirrhosis occurs, the liver will shrink down and pain will subside
Modified Child-Pugh Classification: One point assigned
Probably dont need to know
- Ascites: Absent
- Bilirubin: < 2
- Albumin: >3.5
- Prothrombin time: 1-3
- Encephalopathy: None
Probably dont need to know
Modified Child-Pugh Classification: Two points
Probably dont need to know
- Ascites: Slight
- Bilirubin: 2-3
- Albumin: 2.8-3.5
- Prothrombin time: 4-6
- Encephalopathy: Grade 1-2
Probably dont need to know
Modified Child-Pugh Classification: Three points
Probably dont need to know
- Ascites: Moderate
- Bilirubin: > 3
- Albumin: < 2.8
- Prothrombin time: >6
- Encephalopathy: Grade 3-4
Probably dont need to know
Hepatic dysfunction Causes
- Fatty liver disease (Non-alcoholic fatty liver disease, Nonalcoholic steatohepatitis)
- Infection (Hepatitis)
- Cirrhosis of the liver (Compensated vs decomp)
- Liver failure (Acute, Endstage)
Complications of hepatic dysfunction
- Jaundice (Billirubin build up)
- Portal hypertension
- Varicies (esophgeal)
- Acities
- Hepatic encephalopathy and coma
- Nutritional deficiencies (Often with alc)
Jaundice: Hepatocellular
- Yellow or greenish-yellow sclera and skin (Not too much discoloration)
- Bilirubin levels greater than 2
- Most commonly associated with liver disease
- Dmg liver cells from infection, excessive alc use, and prolonged obstructive jaundice
- Mild to severely ill
- Lack of appetite, N+V, weight loss
- Malaise, fatigue, weakness
- HA, chills , fever, infection
Jaundice: Obstructive
- Yellow or greenish-yellow sclera and skin
- Bilirubin levels greater than 2
- Most commonly associated with liver disease
- Extrahepatic (Gallstones, inflammatory processes, tumor)
- Intrahepatic (Stasis, thickening of bile in canaliculi)
- Dark orange/brown colored urine, Clay colored stool
- Indigestion and intolerance of fats, impaired digestion
- Pruritus
- Skin excoriation from scratching (Jaundice makes you itchy)
More jaundiced than other forms of jaundice
Jaundice: Hemolytic
- Yellow or greenish-yellow sclera and skin
- Bilirubin levels greater than 2
- From the breakdown of RBC
Portal hypertension
- Obstructed blood flow through the liver results in increased pressure throughout the portal venous system
- Causes Ascites
- Causes Esophageal and gastric varices
- Splenomegaly sometimes too
(Essentially due to this pressure, it forces fluid to follow the path of least resistance and go where it normally woudnt )
Ascites
Caused by portal hypertension
* Decreased serum osmotic pressure with movement of albumin from intravascular space to extravascular space including peritoneal cavity: Peripheral edema and ascites
* Genital swelling
* Can also occur from cancer, Kidney disease and HF
Essentially albumin gets moved into peritoneal space and water follows it
Assessment of ascites: Measurement
- Record the abdominal girth and weight daily (Can have rapid weight gain and fluid buildup)
Assessment of ascites: Abdomen
- Striae
- Distended veins (Caput medusae)
- Abdominal hernia
Assessment of ascites: Assessment for fluid
- percussion for a shifting dullness (Dullness=fluid)
- Fluid wave
Assessment of ascites: Dyspnea
Dyspnea can occur with ascites for 3 main reasons
1. Anemia
2. Fluid is pressing on the diaphragm, limiting expansion
3. Fluid has moved into the pleural cavity, causing a pleural effusion
Assessment of ascites: Electrolytes
Monitor for potential fluid and electrolyte imbalances
* Sodium: Reabsorbed by the kidney
* Potassium is often imbalanced
* Renal function
Fluid wave test
Test for ascites
* Pt puts hand midline and then the nurse presses on one side, if fluid is in the abdomen you are able to feel it on the opposite side, if not its not fluid
Dullness
Fluid, and it should shift with gravity with ascites
Mgmt of ascites
- Low sodium, fluid restrictions ( People hate this)
- Diuretics (Spironolactone is the choice, also furosemide)
- Bedrest (During exasperations, standing up causes fluid retention, as ADH levels increase, bed rest helps ya pee)
- Paracentesis (Draining the abdomen, can cause hypotension)
- Administration of salt poor albumin
- Transjugular intrahepatic portosystemic shunt (TIPS) (Shunt to help with portal hypertension)
- Peritoneal drains
What med is used with ascites and why
Spironolactone: First line therapy due to its K+ sparing effects
Spironolactone
K+ sparing diuretic
Blocks the activity of aldosterone, increasing urination and sodium excretion
Decreased overall fluid volume
Can be given with furosemide to decrease K+ levels
Spironolactone: Side effects
- Mild
Hyponatremia, Hypomagnesemia, hypocalcemia, abdominal pain, N+V, leg cramping, dizziness, lightheadedness, male gyno - Serious
Hyperkalemia, hypotension , decreased kidney function, anaphylaxis, steven johnson syndrome, toxic epidermal necrolysis
Esophageal varices
- Occurs as liver disease progresses
- Dilated, knotty veins of esophagus and stomach that develop due to portal vein hypertension and obstruction of portal venous circulation
- Manifestations: GI bleeding hematemesis, melena and hemorrhagic shock
- Prevention: Pt with cirrhosis should undergo screening endoscopy every 2-3 years to monitor for varices
GI bleeding is main thing, they are vomiting alot of blood
mgmt of esophageal varices
- Balloon tamponade (Needs sedation), saline lavage (Cold water on the bleeding wound)
- ICU most likely
- Treat hemorrhagic shock (ABC)
- Oxygen, maintain Airway may need intubation
- IV fluids, electrolytes, volume expanders and blood products
- Vasopressin, Somatostatin, Octreotide
- Nitro in combo with vasopressin to reduce coronary vasoconstriction
- Propranolol and nadolol (Beta blockers), decreasing portal pressure
Surgical mgmt of varices
- Endoscopic sclerotherapy
- Endoscopic variceal ligation (Esophageal banding, placing a band to stop blood flow to that area)
- Transjugular intrahepatic portosystemic shunt (TIPS)
- Surg mgmt
Hepatic Encephalopathy (HE) and coma
- Life threatening issue
- Two main issues: HE and coma
1. Hepatic insufficiency
2. Portosystemic shunting - Accumulation of ammonia levels in the blood (Ammonia enters the brain and causes neuro changes)
- Early signs: Mental status changes and motor disturbances
Hepatic insufficency
Cause of Hepatic Encephalopathy and coma
inability for the liver to detox toxic by products of the metabolism (ammonia)
Portosystemic shunting
Cause of Hepatic Encephalopathy and coma
Collateral vessels develop allowing elements of the portal blood (Filled with toxins extracted by the liver) to enter they systemic circulation
Assessment and Stages of Encephalopathy
Assessment
* EEG
* Changes in LOC and motor function (First sign)
* Potential seizures
* Fetor hepaticus (Poop breath) asterixis (Flappy wrist)
* Monitor fluid, electrolyte and ammonia levels
Stages
* 1-4
Stages of Encephalopathy: Stage 1
- Normal LOC with periods of lethargy and euphoria
- Reversal of day night sleep patterns
- Impaired writing and ability to draw line figures
- Normal EEG
Stages of Encephalopathy Stage 2
- Increased drowsiness
- Disorientation
- Inappropriate behavior
- Mood swings
- Agitation
- Asterixis
- Fetor hepaticus
- Abnormal EEG with generalized slowing
Stages of Encephalopathy: Stage 3
- Stupor: Difficult to rouse
- Marked confusion
- Incoherent speech
- Asterixis
- Absent deep tendon reflexes
- Rigidity of extremities
- EEG markedly abnormal
Stages of Encephalopathy: Stage 4
- Comatose, may not respond to painful stimuli
- Absence of asterixis
- Absence of deep tendon reflexes
- Flaccidity of extremities
- EEG markedly abnormal
Mgmt of Hepatic Encephalopathy
- Reduce protein intake
- Reduction of ammonia from systemic circulation by gastric suction, lactulose, enemas, oral antibiotics (Kill ammonia producing bacteria in gut)
- Discontinue sedatives, analgesics and tranquilizers and any other med which can affect liver function
Fatty liver disease
- Lipids accumulate in hepatocytes
- NAFLD
- NASH
- Combination of obesity and heavy drinking -> severe liver dmg (Can take 20-30 yrs to develop into ESRD)
- Those at risk should be monitored closely for S+S liver dysfunction
Obesity and drinking
Fatty liver disease
- Lipids accumulate in hepatocytes
- NAFLD
- NASH
- Combination of obesity and heavy drinking -> severe liver dmg (Can take 20-30 yrs to develop into ESRD)
- Those at risk should be monitored closely for S+S liver dysfunction
Obesity and drinking
Non-alcoholic fatty liver disease (NAFLD)
Less serious than NASH
Associated with obesity
Non-alcoholic steatohepatitis
More serious than NAFLD
Results in dmg, fibrotic changes in the liver (Cirrhosis)
Assosiated with obesity
Viral hepatitis
- ABCDEG
- Causes necrosis and inflammation of liver cells, resulting in liver enlargement and obstruction of blood flow to the liver
Non-viral hepatitis
- Toxic and drug induced
- Alc, hepatotoxic chemicals, Botanical agents
- S+S: Anorexia, N+V, jaundice, hepatomegaly, bleeding, chills, fever, rash, pruritus
- Recovery unlikely of prolonged period, with exposure and symptoms
Acetaminophen, mushrooms, carbon tetracholoride
Fecal oral hepatitis
A/ E
Common findings in hepatitis
- Flu like symptoms (Fatigue, Decreased appetite, N, Ab pain, joint pain)
- Physical (Fever, vomiting, dark colored urine, clay colored stool, jaundice)
Types of hepatitis: Type A
General info
- Source: Feces
- Route of transmission: Fecal oral
- Chronic infection: No
- Prevention: Pre and post immunizations
Types of hepatitis: Type B
General info
- Source: Blood, blood derived bodily fluids
- Route of transmission: Percutaneous membranes
- Chronic infection: Yes
- Prevention: Immunization
Types of hepatitis: Type C
General info
- Source: Blood, Blood derived body fluids
- Route of transmission: Percutaneous permucosal
- Chronic infection: Yes
- Prevention: Blood donor screening , risk behavior modification
Types of hepatitis: Type D
General info
- Source: Blood/ blood derived body fluids
- Route of transmission: Percutaneous permucosal
- Chronic infection: Yes
- Prevention: Immunizations, risk behavior modification
Cant have D without B
Types of hepatitis: Type E
General info
- Source: Feces
- Route of transmission: Fecal oral
- Chronic infection: No
- Prevention: Ensure safe drinking water
Hepatitis A: HAV
- Spread by poor hand hygiene or sanitation **Fecal oral **
- Ingestion of contaminated food or water, especially shellfish
- Contact with infected stool (Incontinence, anal sex)
- Hep A antibodies reveal presence of Hep A
- S+S: Mild flu like symptoms, low grade fever, anorexia, later jaundice , and dark urine , indigestion and epigastric distress enlargement of liver and spleen
- Mgmt: Bedrest during acute stage, and supportive care
Not chronic
Hepatitis A: HAV
- Spread by poor hand hygiene or sanitation **Fecal oral **
- Ingestion of contaminated food or water, especially shellfish
- Occurs often with food service industry
- Contact with infected stool (Incontinence, anal sex)
- Hep A antibodies reveal presence of Hep A
- S+S: Mild flu like symptoms, low grade fever, anorexia, later jaundice , and dark urine , indigestion and epigastric distress enlargement of liver and spleen
- Mgmt: Bedrest during acute stage, and supportive care
Not chronic
Prevention and mgmt of hep A
- Hep A immunization
- Immune globulin for passive immunity to close contacts, non-immune and institutionalized
- Good handwashing, safe water and proper sewage disposal
- No treatment except supportive
Hep B: HBV
- Transmitted via: Blood, saliva, semen , and vaginal secretions, STI, transmitted to infant at birth
- Major cause of cirrhosis and liver cancer (Chronic infections)
- Manifestations: Insidious and variable, similar to hep , loss of appetite, dyspepsia, ab pain , aching, malise and weakness, +/- jaundice (Clay colored stool, dark urine
- Hep B antigen indicates a person is infectious, chronic carriers are infectious
- Can be chronic
Mgmt of hep B
- Acute infection: no meds, supportive care
- Chronic infection: They are unable to clear the virus and given antivirals are needed
- Bedrest and nutritional support
- Passive immunization with hep B immune globulin
- Vaccine is available
Hep C: HCV
- Transmission is via blood
- 1/3 cases of liver cancer are caused by this and is the #1 reason for liver transplant
- Risk factors are the same for Hep B, Blood and all that
- Symptoms are usually mild if at all
- Can have the disease and not know they have it, leading to transmission to others
- Chronic cases are common
Mgmt of Hep C
- No found benifit to rest, vitamins and diet
- Give Direct acting antivirals, can be undetectable and cured 8-12 weeks of completed treatment
- Alc progresses diseases, pt cannot drink when they have hep C
- Meds that affect the liver should be avoided
Direct acting antivirals
- Newer med that is given for hep C
- Destroys the virus directly, preventing further replication
- More effective than prior antivirals, less side effects
- Can be undetectable and cured in 8-12 weeks
Simeprevir, sofosbtavit, paritaprevir, glecaprevir, grazoprevir
Hep D: HDV
- Main thing is you cant have Hep D without B (Needs the hep B antigen)
- Blood and sexual contact transmission, injectable drugs, hemodialysis and recipients of multiple blood transmission
- S+S similar to hep B, but more likely to develop acute, fulminant liver failure or chronic active hepatitis and cirrhosis
- High dose interferon For ONE year
Hep E: HEV
Fecal oral transmission, contaminated water mainly
* Resembles hep A, self limiting, abrupt onset, not chronic
* No treatment except supportive care
T/F only persons with Hep A can get Hep E
False, only pt with hep B can get hep D
Alcoholic Cirrhosis
Scar tissue surrounds the portal areas, most common
Post necrotic Cirrhosis
Broad bands of scar tissue across the liver
Biliary cirrhosis
Scarring occurs in the liver around the bile ducts
Occurs from chronic biliary obstruction
Hepatic Cirrhosis: Patho
Replacement of normal liver tissue with diffuse fibrosis
Liver becomes fibrotic and nodular
Manifestations of hepatic cirrhosis
- Liver enlargement (Shrinking later into the disease, when fibrosis progresses)
- Portal obstruction
- Ascites
- Infection/peritonitis
- Varices
- Edema
- Vitamin deficiency
- Anemia
- Mental deterioration
Common drugs that are assosiated with liver failure
Probably dont need to know
- Acetaminophen
- Alc
- Coke
- Nsaids
- Kava Kava
- Mushrooms
Liver transplant success
Depends on successful Immune suppression
What is used to allocate cadaver livers
MELD score
Graft vs host disease
- Rejection of transplanted liver
- S+S of acute liver injury like inflammation of liver
Liver transplant criteria
- Stringent criteria if they have primary liver cancer, small early lesions (1 x < 5 cm or 3 x < 3 cm)
- End stage liver disease: whole liver from deceased donor or partial liver from live donor
What lobe of the liver is donated in a live liver transplant
Right
Immunosuppressants given for liver transplant
- Cyclosporine
- Tacrolimus
- Sirolimus
- Everolimus
- Mycophenolate
Corticosteroids are only given when neeeded, (Induction or rejection)
Immunosuppressants given for liver transplant
- Cyclosporine
- Tacrolimus
- Sirolimus
- Everolimus
- Mycophenolate
Corticosteroids are only given when neeeded, (Induction or rejection)
Where is jaundice first seen
Sclera of the eye
Education for viral hep
- Contact precautions
- Educate pt and fam about preventing transmission
- Avoid sex until hep antigen testing is neg
- Use proper hand hygiene and contact precautions
- Refer for substance abuse program
- Avoid alc and injection drugs
- Needle syringe exchange programs
Liver failure /disease education: Resp care
- Comfort measures by positioning pt to ease resp effort (Can be difficult due to presence of ascites
- Sit in a chair or elevate HOB 30 degrees with feet elevated (Lay them flat during the acute period)
- Oxygen, deep breathing and coughing
- Call for changes in resp status (Can indicate pleural effusion)
Liver failure /disease education: Skin integrity
- Measures to prevent pressure injuries (T/P 2 hrs)
- Reduce pressure points
- Monitor for skin breakdown (Especially with peripheral edema)
- Measures to alleviate pruritus (Gentle skin care, avoid soap, washing with cool water, applying lotion to decrease the itching, keep lotion in the fridge
- Assess for excoriations bruising, petechiae, jaundice
Liver failure /disease education: Nutrition
- High carb, high cal, moderate fat/protein and low sodium
- Vitamin supplements (Thiamine, folate, multivitamins)
- Small frequent meals
- Proper positioning during meals
- Label reading for salt content, don’t add salt to food
Liver failure /disease education: Fluid balance
Monitor and measure increasing abdominal distension, peripheral edema
Keep I+O daily weights
Restrict fluids if prescribed
Liver failure /disease education: Activity
- Bedrest during acute illness
- Planned exercise and rest periods
Liver failure /disease education: Neuro status
- Monitor and call for deteriorating mental status and dementia consistent with hep encephalopathy
- Monitor for asterixis and fetor hepaticus
- Lactulose if elevated ammonia level/ hepatic encephalopathy to reduce ammonia
Liver failure /disease education: GI status
- If ascites measure abdominal girth daily
- Observe for potential bleeding, from varices (S+S: Anxiety, restlessness, Tachycardia, N+V, Hematemesis, melena)
- Pain mgmt: Based on provider, analgesics, antacids acid blockers, antiemetics
